Human behaviour is complex. The use of a  biological or medical model is ne of the
approaches used to understand its intricacies.

The biological approach examines the roles of
physiology- the brain and other organs’ reactions influenced by chemicals and
the control of certain motor functions, ontogeny – or how a pattern of
behaviour develops over a period because of genetics and experiences, evolution
– for instance, the reasons as to why certain functions exist even though their
relevance today is questionable and functionality – or why structures have
evolved the way they have (Tinbergen 1951). 

Abnormal behaviour, as broadly defined by the American
Psychological Association is the occurrence of a clinically significant pattern
of behaviour that causes distress or disability which has a greater risk in
resulting in death, disability or the loss of one’s freedom. The purpose of this essay is to
attempt to explain the occurrence of abnormal behaviour in the context of
two biological factors; genes and neurotransmitters.

The question as to whether a set of behaviour has been
inherited or is a result of environmental factors, or both, has been long
debated over. For it to be determined that an individual’s genotype is indeed
the sole reason for the resulting behaviour, it must be proven that no other
environmental contributor is evident as a causal factor.

According to Plomin et al. (1994) research conducted using
both identical and fraternal twins, show results of a greater genetic influence
on behavioural disorders such as schizophrenia, major affective disorders and
antisocial personality disorder as opposed to medical conditions such as
Parkinson’s disease or Rheumatoid Arthritis. Further studies conducted in
behavioural genetic research also signifies that the findings pertaining to the
influence of environmental factors in adoptive sibling studies note that a
shared environment has no bearing on the manifestation of psychological traits
(Plomin et al – 1994: 1735 and McGue and Bouchard 1998:5). There is no conclusive evidence to date, to
suggest that genetics is the only constant in resulting abnormal behaviour. The
reason for this could be due to the fact that the study of the approximately
30,000 human genes, is still a work in progress. It has been said that once
decoded one would be able to access the data of every aspect of what determines
the development of human beings (Human Genome Project 2001)

Consider the current research available on anti-social
behaviour (ASB) for instance.  There is no denying that genetics play
a role in its occurrence (Raine 2008: 323-324).  In fact, it has been
determined that genetic influence accounts for more than 50% of resulting
anti-social behaviour (Moffit 2005: 535). However the variance at play here is
attributed to environmental factors. Of the two methods used to evaluate the
influence of environmental factors in resulting anti-social behavior, one, is
the hypothesis that MZ twins’ genetic construct (being twice as similar than
that of DZ twins), should result in a greater similarity if tested for symptoms
of such behaviour. If this didn’t indicate such a similarity, then it is
reasonable to assume that that other factors may have influenced the increase
in the levels of similarity. Although found to be conclusive of several other
abnormalities, this didn’t hold true with anti social behaviour (ASB). 

In a study conducted by Kendler et al (2003) on the influence of genetic risk and
environmental risk involved in common psychiatric and substance use disorders,
it was discovered that environment played a more significant role in resultant
ASB as opposed to experiencing anxiety and engaging in substance abuse. Further
studies conducted to ascertain the occurrence of ASB indicative by aggression
and rule-breaking, by using behavioural genetics biometric modelling, has shown that both
genetics and environment simultaneously play a role in its occurrence and while
between the ages of 9 and 10 its effects are a 41% – 40% – 19% split (genetics
to shared environment to non-shared environment), with the 14-15 age group this
was found to shift to a 44% – 79% in a bias towards environmental factors. It
can be said that age too therefore, may play a role in antisocial behaviour
(Niv et al 2003).

The Serotonin Transporter gene is one of the most
studied variants in psychiatry and neuroscience. It was discovered that an
anomaly in the 5-HTTLPR section of the Serotonin Transporter gene affects the
reabsorption of Serotonin after its release. In a study conducted among 847
participants, the existence of two variants ( long and short), of this gene was
discovered. When tested in conditions of highly stressful events experienced by
participants aged 21 -26, it was found that the individuals with two short
forms of the gene had a greater tendency to develop depression when subjected
to such stressful event over a span of time. The short gene by itself didn’t
cause depression, but increased the individuals’ susceptibility to getting it,
when faced with stressful events (Caspi et al 2003).  A more recent
gene x environment x mood (GEM) study further revealed that a significant G X E
interaction resulted in a greater predisposition for depression. It was also
revealed that age and gender played key roles in resulting depression (older
adolescent carriers of the short allele subjected to peer pressure over a
course of time and females subjected to similar peer pressure, were more prone
to be diagnosed with it) (Hankin et al 2015: 804-812).

Effects of the existence of this genetic anomaly has
also been observed in individuals with a predisposition to psychopathy. In a
study carried out to determine the extent of the influence of the serotonin
transporter gene in relation to impulse control ( a common trait of
psychopathy), and its behavior  in relation to  G X E conditions of
callousness and narcissism, it was found that individuals who had the s/s
allele rated high on the APSD (Antisocial Process Screening Device) scale on
impulsiveness, whereas those with the l/l allele raised in low
socio-economic  environments indicated a greater disposition towards
callousness and narcissism. The research also indicated that no correlation was
seen to exist between low socioeconomic status and the existence of the genetic
anomaly (Sadeh et al 2010: 604-608).

The premise of the theories associated with
neurotransmitters is, that it influences chemical imbalances that result in
abnormal behaviour (Sue et al 2010:38). More specifically, studies have
revealed that many endogenous compounds such as acetylcholine (ACh), dopamine
(DA), serotonin (5HT), gamma aminobutyric acid (GABA) and norepinephrine (NE) –
(among those more commonly referenced), are said to influence the occurrence of
several abnormal conditions or psychiatric states such as schizophrenia, depression
(Hanin 1978: 135-138), and more recently in aggressive behaviour (Narvaes et al
2014:601-607) and psychopathy (Buckholtz et al 2010: 419-421). 

 Consider the complexities of schizophrenia for
instance. After over 1200 studies in trying to understand the reason for its
occurrence it has been determined that no one gene but the existence of several
susceptible genes code for varying molecular abnormalities that influence
insufficient information processing that results in a genetic predisposition towards
schizophrenia (Stahl 2007 cited in Sue et al 2010: 375). In a more recent study
conducted to understand the influence of these underlying genes, 14 genes
responsible for a combination of neurotransmission and functional
inconsistencies were fund to be present in cases of schizophrenia. Of these 14
genes, primarily featuring on the list were three genes responsible for the
neurotransmission of GABA. This data could explain the abnormal EEG gamma band
activity detected in schizophrenic patients.  The experiments were carried
out by administering PCP and clozapine in a ‘pharmacogenomic mouse model’ and
analysed against comparative genetic linkage and post-mortem brain data to
arrive at these findings (Le-Niculescu et al 2007).

Depression, has long been a subject of psychiatric
research. The monoamine hypothesis of depression was first observed as a result
of the effects caused by two monoamine oxidase inhibitors, namely iproniazid
and imipramine, in non-psychiatric patients. The compounds had a marked impact
on the transmission of serotonin causing significant anti-depressant effects.
Furthermore, it was observed that Reserpine caused depressive symptoms in
others. To date, antidepressant agents are designed to influence monoamine
transmission by inhibiting either neural reuptake or degradation.

Aggressive behaviour, a trait associated with
psychopathy, which in turn results in criminal behaviour, has given cause to
greater scientific research as its social and economic burden is immense.
Monetarily in the US alone this is indicative to exceed $1 trillion (Buckholtz
et al 2010). There is now, documented research confirming the roles of
neurotransmitters such as GABA, dopamine and serotonin existent in in
individuals prone to exhibiting aggression (Narvaes et al 2014). 

Further to this point, in a study carried out to determine
the hypersensitivity of the dopamine reward system in individuals with
psychopathic traits (of which aggression is one),  dopamine was found to be a key determiner in
the occurrence of an impulsive-antisocial temperament (aggression) indicating
increased interaction with the mesolimbic dopamine system in response to
reward. Furthermore, several studies conducted on rodents in preclinical tests
also indicate mesolimbic dopamine to be critical in the expression of
aggression (Buckholtz et al 2010).               

In reviewing the genetic and neurochemical premises of
abnormal behaviour, we find that neither one nor the other can be designated as
the sole cause of the resulting abnormal behaviour. There is evidence in
several resultant abnormal patterns of behaviour to suggest that genetic
predisposition plays a role in creating susceptibility among individuals in
relation to certain chemical functions. As referenced for instance with
schizophrenia the existence of three genes responsible for the transmission of GABA
was observed. With aggressive behaviour and resultant psychopathy, we see a
predisposition towards delinquent behaviour because of a polymorphism of the
serotonin transporter gene and a heightened interaction of the mesolimbic
dopamine system in response to reward. With depression, the existence of two
short alleles of the serotonin transporter gene indicated a greater probability
of encountering depression. Although monoamine based anti-depressants are the
first course of therapeutic measures, certain gene polymorphisms significantly
contribute towards a depressed individual’s efficacy in relation to
anti-depressants (Uhr et al 2007).

Furthermore, although not previously discussed in this essay,
it should be noted that abnormal behaviour, can also be attributed to other
factors. Evolution, for example. Take the evolutionary predisposition to fear
certain species such as snakes and spiders resulting in present day phobias of
the same (Ohman and Mineka 2001). Abnormal behaviour can also be the result of
the formation or structure of the brain – consider anti-social behaviour for
instance; there is mounting evidence to suggest impairments to the brain’s
prefrontal cortex in individuals who exhibit such traits (Raine and Yang 2006);
in fact, it’s been found that murderers show reduced glucose metabolism in this
area of the brain when faced with a task that’s meant to activate it (Raine 2008).
With schizophrenia, according to the neurodevelopmental hypothesis,
abnormalities in the brain has not only been attributed to genetics but also to prenatal or
postnatal development and environmental influences, known to aggravate its
symptoms (Weinberger 1996). It was also found that among a group of 390
individuals with schizophrenia,abnormalities were present in the left temporal
and frontal areas of the cortex and that the thalamus appeared to be smaller
than average(Harms et al 2007).

Environmental factors too play a key role – some of
which was touched on in this essay previously. Further to  this point, consider that in cases of
depression,  although the susceptibility in getting it is greater for
individuals who have the short serotonin transporter gene, the existence of
other genes that increase the probability of acquiring depression and are
triggered by an individual’s traumatic upbringings, have been found to be
present in some patients with depression (Bradley et al 2008 and Haeffel et al
2008). Some cases of depression have also been linked to viral infections such
as Borna disease (Kalart 2010: 439) and yet some others could be the result of
giving birth – statistics state that at least 20% (Hopkins et al 1984 cited in
Kalart 2010: 440) of women report some level of postpartum depression.

Thus, the explanation of the complexities of abnormal
behaviour must be approached from a broader perspective, for it to be
comprehended to some degree.  



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